ArticleJournal of nanobiotechnology2026
Cardiac-targeted delivery of miRNA via antioxidant nanozymes ameliorates cardiac dysfunction and fibrosis after myocardial infarction.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Despite advances in reperfusion therapy, treatment outcomes for myocardial infarction (MI) remain limited by poor targeting specificity and insufficient bioavailability of therapeutic agents in the ischemic myocardium. Here, we report CCTP-miR@CTP, a non-liposomal nanozyme platform that integrates cardiomyocyte-targeted delivery, intrinsic catalytic antioxidant activity, and therapeutic miRNA delivery within a single multifunctional system. In vitro, CCTP loaded with miR-26a mitigated H₂O₂-induced ROS accumulation, restored mitochondrial membrane potential, and suppressed autophagy and apoptosis in cardiomyocytes. In vivo, CCTP-miR@CTP preferentially accumulated in the infarcted myocardium, where it reduced infarct size, improved cardiac function, suppressed inflammatory responses, promoted angiogenesis, and attenuated extracellular matrix deposition and myocardial fibrosis. Mechanistically, CCTP not only served as an effective nucleic acid carrier but also coordinated redox homeostasis and cell survival pathways, amplifying the therapeutic efficacy of miRNA-based intervention. This study presents a material-design strategy to improve miRNA druggability in cardiovascular medicine and identifies CCTP-miR@CTP as a candidate nanotherapeutic for MI.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.